Genetic control of Blattella germanica

Based on a literature survey, the possibilities of a genetic control of the German cockroach (Blattella germanica) are shown. First, an oversight is given on the cytogenetics of the German cockroach, including some important mutations. Then the control methods by genetic mechanisms are explained. This chapter begins with analysing the relevant biological pecularities. In control measures, the dominant lethal mutations (induced by rays rich with energy and by chemosterilants) have only a chance if they can be applied in the scope of autosterilization of natural populations. Reciprocal translocations may expect maximum consideration in the future of the control of the German cockroach. Some of these are already available in the heterozygote state. But the establishment of homozygous strains was not yet successful up to now. The possibilities of the application of translocation-heterozygotes are discussed. Such mutant strains of cockroaches which bear several translocations in the heterozygous state, offer the most promising way of control. This may even include the population's eradication. A long-lasting regulation of the population may be achieved with the introduction of insects mutated in this manner even in the case if a complete eradication is not attainable. It might be expected that also other genetic mechanisms may contribute, in future, to the improvement of cockroach control. Such mechanisms may be conditional lethal factors, sex distortions, and others more.     

基因控制和活化生物材料的研究与进展

目的从分子水平上来研究与开发生物材料,特别是生物技术和基因工程的原理与方法的运用.方法综合最近的有关研究和文献资料,从理论与实践相结合的方法阐述了生物材料学三个方面的研究进展.结果指出了基因工程材料的发展趋势.结论从分子水平上来研究与开发生物材料是目前研究的一个热点问题,使从分子水平上来研究与设计材料成为可能并提供了广阔的空间.     

Genetic control of severe pre-eclampsia.

A genetic analysis has been made of published and new data on the familial occurrence of severe pre-eclampsia in primigravid women. This has shown that the condition may be largely a Mendelian recessive one. Bcause the condition occurs only in pregnancy, and because susceptible women cannot otherwise be identified, it is difficult to decide whether the genotype of the parent or of the offspring carried in utero leads to the condition. Data on the incidence of severe pre-eclampsia in the relatives of women who have suffered eclampsia support the maternal genotype hypothesis, while similar data, in which the index cases were women who had had severe pre-eclampsia, are more compatible with the fetal genotype hypothesis. Data on the incidence of the condition in blood relatives of index cases compared to the incidence in their corresponding in-laws are now required. Such a comparison would allow a choice to be made between the two hypotheses if one or the other were correct, or would assess the contribution of each if a genotype X genotype interaction were involved. Recurrent severe pre-eclampsia seems to have the same genetic basis as the more common primigravid type. However, mild, that is non-proteinuric, pre-eclampsia usually seems to be inherited independently of the severe form.     

基因控制和活化生物材料的研究与进展

目的 从分子水平上来研究与开发生物材料，特别是生物技术和基因工程的原理与方法的运用。方法 综合最近的有关研究和文献资料，从理论与实践相结合的方法阐述了生物材料学三个方面的研究进展。结果 指出了基因工程材料的发展趋势。结论 从分子水平上来研究与开发生物材料是目前研究的一个热点问题，使从分子水平上来研究与设计材料成为可能并提供了广阔的空间。     

Genetic control of survival in epidemics

Descendants of Dutch colonists, who emigrated to Surinam in the last century and survived epidemics of typhoid and yellow fever with a total mortality of about 60%, were tested for twenty-six polymorphisms. The gene frequencies were compared with those of a large Dutch control sample. An analysis of drift indicated that the variations in gene frequencies observed for C3, Gm, HLA-B, and GLO were unlikely to be due to drift. Therefore these data might indicate selection through genetic control of survival in these epidemics.     

Genetic control of susceptibility to autoimmune gastritis

A familial component to the tendency to develop autoimmune gastritis has long been recognized. Although linkage to certain HLA alleles and an association with the endocrine autoimmune diseases thyroiditis and type 1 diabetes have been reported, little further progress has been achieved in clinical studies. In contrast, the mouse model of gastritis induced in the BALB/c strain by thymectomy in the third day of life has identified four linkage regions; two on distal chromosome 4 (Gasa1 and Gasa2), one on chromosome 6 (Gasa3) and one in the H2 (Gasa4). Three of these four genes colocalize with NOD mouse diabetes susceptibility genes--the strongest concordance identified to date between any two autoimmune diseases--reflecting the association between autoimmune diabetes and type 1 gastritis in humans.     

Genetic control of methanol utilization in yeasts

Considered are our own data and those found in literature on the properties of yeast mutants impaired in their ability to utilize methanol as sole carbon and energy source; hypotheses about the role of alcohol oxidase and citrate synthase in biogenesis of peroxisomes are proposed. It has been proved that formaldehyde reductase participates in the control of the formaldehyde level in the cell. Properties of mutants defective in the catabolite repression and inactivation of enzymes of methanol metabolism are described. The existence of several autonomous mechanisms of the catabolite repression of alcohol oxidase has been shown. It has been found, that the induction of glyoxysomal enzymes of C2-metabolism is repressed by methanol in the ecr1 mutant of Pichia pinus with the affected repression of alcohol oxidase by ethanol. Data are presented on the regulatory properties of the recently discovered acidification system of the medium induced by methanol. Such acidification occurs due to symport extrusion of protons and formate anions from the cells.     

Genetic control of mouse cytomegalovirus-induced myocarditis.

Mouse cytomegalovirus (MCMV) infection of mice induced myocarditis, characterized by a mononuclear cell infiltrate with associated necrosis of myofibres. Myocarditis was observed in parallel with viral inclusion-bearing cells in the heart during the acute phase of the infection. Myocarditis also persisted after the acute phase when viral antigens were no longer detectable by immunoperoxidase histochemistry and infectious virus could not be cultivated from various organs. The influence of host genetic factors on the development of cytomegalovirus-induced myocarditis was investigated using H-2 congenic and recombinant inbred mouse strains. Analysis of congenic variants with C57BL/10 and BALB/c backgrounds and the A/J strain revealed that genes linked to the H-2 complex influenced susceptibility to peak levels of MCMV-induced myocarditis seen 7 and 10 days post-infection. In addition, non-H-2 genes of the BALB/c background were important in determining the severity of myocarditis. Analysis of the strain distribution pattern of the CXB recombinant inbred series did not disclose the identity of the BALB/c non-H-2-linked allele conferring susceptibility to MCMV-induced myocarditis. The level of myocarditis seen in the F1 hybrid between the high-responder BALB/c and low-responder C57BL/6 strains suggested dominant inheritance. The amount of viral replication in the major target organs did not correlate with the severity of myocarditis. In conclusion, at least two genes, one mapping to the H-2 complex and another non-H-2-linked gene, influenced the development of myocarditis in MCMV-infected mice.     

Genetic control over fragile X chromosome expression

The cytogenetic expression of fragile sites is highly variable. Sites are seen in differing proportions of cells. To determine if part of this variability is genetic, the proportions of lymphocytes manifesting the fragile X were examined in a large cohort of males with the fragile X chromosome. The number of fragile X cells was solely determined by genetic factors: the heritability as determined from the correlation between brothers as well as between cousins was 99.6% and 94.4%, respectively, as compared with 0% in unrelated males with the fragile X. This is consistent with pure genetic determination without any environmental influence over the expression of the fragile X chromosome in males.     

Genetic and epigenetic control of levamisole-induced immunostimulation

Antibody responses to a T-cell dependent antigen, sheep red blood cells, were evaluated in mice of various inbred strains, treated or untreated, with levamisole. These responses appear to be under polygenic control, not associated with the H-2 complex, and modified by a Y-linked component and epigenetic factors revealed by aging. Strain, sex, age and the dose of levamisole all in influenced in an interrelated manner the activity of levamisole. Effects varied from inhibited to unchanged or increased antibody-forming cell numbers, without a direct relationship between the genetic regulation of levamisole effectiveness and a genotypic capacity to respond to the antigenic signal. Therefore, a complex relationship between host, antigen and immunopotentiator appears to be responsible for modifying the production of suppressor or helper influences. The present findings may serve as a warning against the uncritical use of levamisole.     

Genetic control of resistance to tumors.

Hybrid resistance to a BALB/c plasmacytoma, MPC-11, has been investigated. The results indicate that heterozygosity within the H-2 complex is neither necessary nor sufficient for resistance to be observed. However, in the presence of a single gene or gene complex which segregates independently of H-2, differential effects of various H-2 haplotypes can be seen. Resistance is radiation-sensitive and silica-insensitive and probably depends on active immune responses. The data also suggest that production by a hybrid of endogenous viral antigens with certain type-specific determinants shared with viral antigens expressed on the tumor may interfere with resistance. The mechanism for this is not understood but might involve tolerance, suppression, or enhancing antibody.     

Genetic control of the tendency to tolerance circumvention

Random bred rabbits were injected with human serum albumin (HA) at birth to induce tolerance to HA. Tolerant animals were then immunized with a p-azobenzenesulfonic acid derivative of human albumin (HA-D₃₁). A proportion of these animals, 42 %, (27/64) responded with the production of antibody to HA-D₃₁ (TCR-responders). Matings were carried out between TCR-responders and between TCR-nonresponders, and the offspring were subjected to the same procedures as their parents. Selective breeding of TCR-responders produced 70 % (12/17) responders after two generations. Selective breeding of TCR-nonresponders produced only TCR-nonresponders after the third generation. Fourth generation offspring of TCR-nonresponders, which were not injected with HA at birth, produced an antibody response to HA-D₃₁. The specificity of this antibody was analyzed by agglutination-inhibition tests and was found to be similar to that of antibody produced in unselected rabbits. The genetic control of responsiveness to HA-D₃₁ in HA-tolerant rabbits is polygenic and autosomal.